Spermatocytic Seminoma Research Articles

Intratubular germ cell neoplasia of the testis: a brief review.

Germ cell tumors of the testis may be divided into 3 broad categories according to age at presentation. The tumors in the pediatric age group include teratoma and yolk sac tumor. These tumors are generally not associated with convincing intratubular neoplasia. The second group consists of tumors presenting in third and fourth decade of life and include seminoma, embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma as well as mixed germ cell tumors. The precursor cell for these tumors is an abnormal gonocyte that fails to differentiate completely into spermatogonia. These abnormal cells stay dormant in the gonad during intrauterine life as well as infancy and childhood, but undergo proliferation during puberty and can be identified as intratubular germ cell neoplasia unclassified (IGCNU). These tumor cells continue to manifest protein expression pattern that resembles primitive germ cells (PLAP, c-KIT, OCT3/4). After a variable interval following puberty, IGCNU cells may acquire ability to penetrate the seminiferous tubules and present as an overt germ cell tumor. Acquisition of isochrome 12 and other genetic abnormalities are usually associated with this transition. The level of DNA methylation generally determines the phenotype of the germ cell tumor. The third type of germ cell tumors is spermatocytic seminoma, which is a rare tumor encountered later in life usually in fifth and sixth decade. The cell of origin of this tumor is probably postpubertal mature spermatogonia which acquire abnormal proliferative capability probably due to gain of chromosome 9 resulting in activation and amplification of genes such as DMRT1. The tumor cells manifest many of the proteins normally expressed by mature sperms such as VASA, SSX2, and occasionally OCT2. Although spermatocytic seminoma may also have an intratubular growth phase, it completely lacks features of IGCNU.

Distribution of testicular tumors in Lebanon: a single institution overview.

Testicular tumors constitute a rare type of cancer affecting adolescents and young adults with recent reports confirming an increase in incidence worldwide. The purpose of this study was to estimate the epidemiological characteristics and histological subtypes of testicular tumors in the Lebanese population according to the WHO classification of testicular and paratesticular tumors. In this single institutional retrospective study, all patients diagnosed with a testicular tumor in Hotel-Dieu de France Hospital University in Beirut between 1992 and 2014 were enrolled. The age, subtype based on the 2004 WHO classification and body side of tumor were analyzed. A total of two hundred and forty-four (244) patients diagnosed with a testicular tumor in our institution were included in the study. Two hundred and one patients (82.4% of all testicular tumors) had germ cell tumors (TGCT). Among TGCT, 50% were seminomatous tumors, 48% non-seminomatous tumors (NST) and 2% were spermatocytic seminomas. The NST were further divided into mixed germ cell tumors (63.9%), embryonic carcinomas (18.6%), teratomas (15.4%) and yolk sac tumors (2.1%). The mean age for testicular tumors was 32 years. The mean age for germ cell tumors was 31 years and further subtypes such as seminomatous tumors had a mean age of 34 years, 28 years in non-seminomatous tumors and 56 years in spermatocytic seminoma. Patients with right testicular tumor were the predominant group with 55% of patients. Three patients (1.2%) presented with bilateral tumors. The distribution of different subgroups and the mean age for testicular tumors proved comparable to most countries of the world except for some Asian countries. Germ cell tumors are the most common subtype of testicular tumors with seminomatous tumors being slightly more prevalent than non-seminomatous tumors in Lebanese patients.

Genome wide DNA methylation profiles provide clues to the origin and pathogenesis of germ cell tumors.

The cell of origin of the five subtypes (I-V) of germ cell tumors (GCTs) are assumed to be germ cells from different maturation stages. This is (potentially) reflected in their methylation status as fetal maturing primordial germ cells are globally demethylated during migration from the yolk sac to the gonad. Imprinted regions are erased in the gonad and later become uniparentally imprinted according to fetal sex. Here, 91 GCTs (type I-IV) and four cell lines were profiled (Illumina’s HumanMethylation450BeadChip). Data was pre-processed controlling for cross hybridization, SNPs, detection rate, probe-type bias and batch effects. The annotation was extended, covering snRNAs/microRNAs, repeat elements and imprinted regions. A Hidden Markov Model-based genome segmentation was devised to identify differentially methylated genomic regions. Methylation profiles allowed for separation of clusters of non-seminomas (type II), seminomas/dysgerminomas (type II), spermatocytic seminomas (type III) and teratomas/dermoid cysts (type I/IV). The seminomas, dysgerminomas and spermatocytic seminomas were globally hypomethylated, in line with previous reports and their demethylated precursor. Differential methylation and imprinting status between subtypes reflected their presumed cell of origin. Ovarian type I teratomas and dermoid cysts showed (partial) sex specific uniparental maternal imprinting. The spermatocytic seminomas showed uniparental paternal imprinting while testicular teratomas exhibited partial imprinting erasure. Somatic imprinting in type II GCTs might indicate a cell of origin after global demethylation but before imprinting erasure. This is earlier than previously described, but agrees with the totipotent/embryonic stem cell like potential of type II GCTs and their rare extra-gonadal localization. The results support the common origin of the type I teratomas and show strong similarity between ovarian type I teratomas and dermoid cysts. In conclusion, we identified specific and global methylation differences between GCT subtypes, providing insight into their developmental timing and underlying developmental biology. Data and extended annotation are deposited at GEO (GSE58538 and GPL18809).

Immunohistochemical Study of Mixed Germ Cell Sex Cord Stromal Tumours in 13 Canine Testes

Mixed germ cell sex cord stromal tumours (MGSCTs) are composed of seminiferous tubules, filled with admixed neoplastic Sertoli cells (SCs) and germ cells (GCs). The aim of the present study was to describe 13 canine testicular MGSCTs and to investigate the histochemical features and the immunophenotype of the neoplastic GCs and SCs. Neoplastic SCs were always diffusely labelled for vimentin (VIM), neuron specific enolase (NSE), inhibin (INH)-α and anti-Müllerian hormone (AMH). Cytokeratins AE1/AE3 (CK) and desmin (DES) were expressed in 6/13 and 8/13 cases, respectively. Neoplastic GCs were labelled for placental alkaline phosphatase (PLAP) in 7/13 cases and for CD117 (KIT) in 8/13 cases, while 10 cases were stained uniformly by periodic acid-Schiff (PAS). Immature canine SCs are known to express CK, DES, INH-α and AMH, while immature GCs are stained by PAS and express PLAP and KIT. This GC phenotype also distinguishes between classical and spermatocytic seminoma, with the latter being negative for these markers. The results of the present study show that both neoplastic SCs and GCs in MGSCTs have a de-differentiated phenotype.

Intra-abdominal Testicular Seminoma

A 49-year-old man married with five children, with no known previous complaint presented to the surgical unit at University Charity Teaching Hospital with complaints of abdominal swelling for 4 months. He had been suffering from anorexia, weight loss during last two months. The patient experienced dragging pain in the hypogastrium during the last two months. On general examination the patient was found to be ill looking and mildly anemic. On local examination an intraabdominal mass was palpable. The abdominal mass was elongated occupying the whole right iliac fossa and extending into the hypogastrium (12 cm x 8cm approximately). The margins were ill defined, surface was irregular and consistency was hard. The lump was fixed with underlying structures and not tender. On examination of the inguinoscrotal region the left testis was found to be in place but the right testis was absent from the left scrotal sac. Our provisional diagnosis was malignant tumor of the right intraabdominal testis. Investigations showed elevated alkaline phosphatase and B-HCG. Sperm analysis and alpha feto protein were within normal ranges. The CT scan showed a huge solid mass arising from the pelvis with calcification, no liver lesions or para-aortic lymph node enlargement (Figure 1A). We went for laparotomy with lower midline incision and found a huge growth occupying the hypogastrium and the right iliac fossa (Figure 1B). The mass was inoperable. The histopathological examination revealed spermatocytic seminoma (Figure 1C). The location of the undescended testis is identified with the probability of carcinogenesis with the intra-abdominal position having the highest risk for malignancy. Painless enlargement of the testis is the common presentation of malignancy in an undescended testis. Rarely, an abdominal testicular tumor can cause abdominal pain, abdominal mass, and haematuria because of adjacent visceral infiltration [1]. Seminomas tumors are extremely sensitive to chemotherapy and radiotherapy [2].

Recent trends in the incidence of testicular germ cell tumors in the United States.

Testicular germ cell tumors (TGCT), which comprise 98% of all testicular malignancies, are the most commonly occurring cancers among men between the ages of 15 and 44years in the United States (US). A prior report from our group found that while TGCT incidence among all US men increased between 1973 and 2003, the rate of increase among black men was more pronounced starting in 1989-1993 than was the rate of increase among other men. In addition, TGCT incidence increased among Hispanic white men between 1992 and 2003. To determine whether these patterns have continued, in the current study, we examined temporal trends in incidence through 2011. Between 1992 and 2011, 21271 TGCTs (12419 seminomas; 8715 non-seminomas; 137 spermatocytic seminomas) were diagnosed among residents of the Surveillance, Epidemiology, and End Results 13 registry areas. The incidence of TGCT was highest among non-Hispanic white men (6.97 per 100000 man-years) followed by American Indian/Alaska Native (AI/AN; 4.66), Hispanic white (4.11), Asian/Pacific Islander (A/PI; 1.95), and black (1.20) men. Non-Hispanic white men were more likely to present with smaller tumors (3.5cm) and localized disease (72.6%) than were men of other races/ethnicities. Between 1992 and 2011, TGCT incidence increased significantly among Hispanic white [annual percent change (APC)=2.94, p<0.0001], black (APC=1.67, p=0.03), non-Hispanic white (APC=1.23, p<0.0001), and A/PI (APC=1.04, p=0.05) men. Incidence rates also increased, although not significantly, among AI/AN men (APC=2.96, p=0.06). The increases were greater for non-seminoma than seminoma. In summary, while non-Hispanic white men in the US continue to have the highest incidence of TGCT, they present at more favorable stages of disease and with smaller tumors than do other men. The increasing rates among non-white men, in conjunction with the larger proportion of non-localized stage disease, suggest an area where future research is warranted.

Biglycan is a novel binding partner of fibroblast growth factor receptor 3c (FGFR3c) in the human testis

Regulation of spermatogonial maintenance in the human testis is currently not well understood. One pathway suggested to be involved is activated by fibroblast growth factor receptor 3 (FGFR3), which is expressed in a subset of spermatogonia. FGFR3-activating mutations have been identified in spermatocytic seminoma, thought to originate from clonal expansion of spermatogonia. In this study we aimed to characterize potential binding partners of FGFR3, and specifically its mesenchymal “c” splice isoform, in human spermatogonia. Based on expression patterns and homology to the binding site, we identified FGF1, FGF2, and FGF9 as the best candidates for natural ligands of FGFR3c in the testis. In addition, we screened non-FGF proteins and found that a proteoglycan biglycan (BGN) contains a sequence homologous to the FGFR3c binding site on FGF1, and is expressed in peritubular cells adjacent to FGFR3-expressing spermatogonia. Experiments in a cell-free system confirmed that BGN binds to FGFR3c and FGF1. In conclusion, our findings further clarify the complex regulation of FGFR3c in the human testis. We postulate that BGN is a factor secreted by peritubular cells to modulate FGFR3c signaling and thus contributes to the regulation of spermatogonial maintenance.

Spermatocytic variant of classic seminoma: a report of five cases and a brief review of the literature.

BackgroundSpermatocytic seminoma is a rare testicular malignancy, appearing in the adult population. It has a good prognosis and a low rate of metastatic potential.ObjectivesWe present five cases diagnosed and treated with radiotherapy at Rambam Health Care Campus in Haifa, Israel.MethodsBetween 1974 and 1996, five patients with stage I spermatocytic seminoma were referred post-orchiectomy to the Northern Israel Oncology Center. All five patients presented with the typical pathological features of the spermatocytic variant of classic seminoma, and all were staged clinically and radiologically.ResultsMean age at diagnosis was 44 years (range 30–58 years). Main symptoms included a palpable testicular mass and/or testicular enlargement. Mean duration of symptoms was 9 months (range 0.5–24 months). Three patients were irradiated to the para-aortic/ipsilateral iliacal lymph nodes (mean total dose 2,500 cGy), one patient with 4,000 cGy. One patient was irradiated to the bilateral iliacal lymph nodes (2,600 cGy). With a median follow-up of 15 years, four patients are alive with no evidence of disease or severe late side effects. One patient developed severe lymphedema and symptomatic peripheral vascular disease, stage IIA prostate carcinoma (hormonal and brachytherapy treatment) and a non-secretory hypophyseal adenoma (surgically removed); he died at the age of 75 due to severe peripheral vascular and coronary heart disease with no evidence of his first or second primaries.ConclusionsPrognosis is excellent and does not differ from classic seminoma. As in the accumulated experience in early-stage, low-risk classic seminoma, we suggest surveillance as the preferred policy.

Cancer testis antigen expression in testicular germ cell tumorigenesis

Cancer testis antigens are encoded by germ line-associated genes that are present in normal germ cells of testis and ovary but not in differentiated tissues. Their expression in various human cancer types has been interpreted as ‘re-expression' or as intratumoral progenitor cell signature. Cancer testis antigen expression patterns have not yet been studied in germ cell tumorigenesis with specific emphasis on intratubular germ cell neoplasia unclassified as a precursor lesion for testicular germ cell tumors. Immunohistochemistry was used to study MAGEA3, MAGEA4, MAGEC1, GAGE1 and CTAG1B expression in 325 primary testicular germ cell tumors, including 94 mixed germ cell tumors. Seminomatous and non-seminomatous components were separately arranged and evaluated on tissue microarrays. Spermatogonia in the normal testis were positive, whereas intratubular germ cell neoplasia unclassified was negative for all five CT antigens. Cancer testis antigen expression was only found in 3% (CTAG1B), 10% (GAGE1, MAGEA4), 33% (MAGEA3) and 40% (MAGEC1) of classic seminoma but not in non-seminomatous testicular germ cell tumors. In contrast, all spermatocytic seminomas were positive for cancer testis antigens. These data are consistent with a different cell origin in spermatocytic seminoma compared with classic seminoma and support a progression model with loss of cancer testis antigens in early tumorigenesis of testicular germ cell tumors and later re-expression in a subset of seminomas.

Histologic Variants of Seminoma Mimicking Lymphatic Malignancies of the Testis

We focused on the clinical and morphologic similarities that may cause a misdiagnosis between histologic variants of seminoma and we highlighted the differences between spermatocytic seminoma and high-mitotic rate seminoma or plasmocytic testicular lymphoma or plasmacytoma of the testis. We emphasized on the difficult points in the differential diagnosis, with a critical review of the literature, reporting a case series to discuss problems in differential diagnosis.

Recent Advances in Understanding the Etiology and Pathogenesis of Pediatric Germ Cell Tumors

Pediatric germ cell tumors (GCTs) are rare neoplasms arising predominantly in the gonads and sacrococcygeal, mediastinal, and intracranial localizations. In this article, we review current knowledge of pathogenesis of pediatric GCTs, which differs from adult/adolescent GCTs. One distinctive feature is the absence of a progenitor stage, such as carcinoma in situ or gonadoblastoma, which are seen in adult/adolescent GCTs, except spermatocytic seminoma. The primordial germ cell (PGC) is the suggested origin of all GCTs, with variations in histology reflecting differentiation stage. Expression of pluripotency transcription factors OCT-3/4, NANOG, and AP-2γ in germinomas/seminomas/dysgerminomas is consistent with retaining a germ cell phenotype. Teratomas, in contrast, develop through a pathway of aberrant somatic differentiation of immature germ cells, and the yolk sac tumors and choriocarcinomas result from abnormal extraembryonic differentiation. In pediatric GCTs, origin is suggested at an earlier developmental stage because of predisposing genetic factors, although responsible genes remain largely unknown. Some extragonadal GCTs have been linked to overexpression of the KIT/KITLG system, allowing for survival of aberrantly migrated ectopic PGCs. Infant gonadal/sacrococcygeal GCTs may be caused by apoptosis-related pathways, consistent with an association with polymorphisms in BAK1. Although recent advances have identified candidate pathways, further effort is needed to answer central questions of pathogenesis of these fascinating tumors.

Genetics of testicular germ cell tumors

Testicular cancer is by far the most common neoplasm among young males between the ages of 20 and 40years and with an increasing incidence rate worldwide. Congenital malformations of the male genitals, such as cryptorchidism or inguinal hernia are established risk factors. Men with a family history of testicular cancer are also associated with an increased risk of the disease. In the testes more than 90 % of tumors develop from germ cells (progenitor cells) and represent a histologically heterogeneous group. Germ cell tumors in extragonadal localizations are rare. Isochromosome i(12p), the typical marker chromosome in testicular germ cell tumors, occurs as an early event in tumorigenesis. Spermatocytic seminoma is a rare variant of germ cell tumors and according to the current classification is a distinct entity with different morphological, clinical and also cytogenetical features compared with other germ cell tumors.

Spermatozytäres Seminom

Spermatocytic seminomas affect 0.3-0.8 per one million men. This tumor is not, as the name might suggest, a variant of classical seminoma but a distinct nosological entity, which differs markedly from all other germ cell tumors in its epidemiology, peculiar morphology, oncogenesis and clinical outcome. There are no racial differences in the incidence and risk factors are completely unknown. Patients are significantly older than is the case for other germ cell tumors with an average of 53.5 years; nevertheless, more than 25% are younger than 40 years. Spermatocytic seminoma arises from differentiated spermatogonia, not from intratubular germ cell neoplasms. The tumor-specific gain of chromosome 9 seems to be the most important event in the oncogenesis. Conventional spermatocytic seminoma consists of three different cell types which give the tumor a highly aggressive appearance, although in actual fact, the tumor has a very favorable outcome, with few reported cases of general metastatic spread. Anaplastic spermatocytic seminoma, a recently described variant, also takes mostly a benign course; however, spermatocytic seminomas combined with sarcomas are extremely malignant.

First case of bilateral, synchronous anaplastic variant of spermatocytic seminoma treated with radical orchifunicolectomy as single approach: Case report and review of the literature

Spermatocytic Seminoma (SS) is less common than the Classic variant, as its incidence ranges between 1.3% and 2.3% of all seminomas. Generally SS is diagnosed in men older than 50 years. The Anaplastic variant of Spermatocytic Seminoma is characterized by an earlier onset when compared to SS, but a benign behavior in spite of its histological patterns similar to Classic Seminoma. We reported the first case of bilateral, largest and synchronous Anaplastic Spermatocytic Seminoma, in a patient treated with radical orchifunicolectomy alone and with long-term follow-up. The currently available data show that Anaplastic SS reveals a clinically benign behavior, and no distant metastases have been reported so far. A close surveillance after surgery could be considered a valid option in the management of this rare testicular neoplasm.

The utility of immunostaining for NUT, GAGE7 and NY‐ESO‐1 in the diagnosis of spermatocytic seminoma

To identify specific positive immunohistochemical markers for spermatocytic seminoma (SS). We studied the reactivity of 94 (total) cases of SS, seminoma, embryonal carcinoma and solid yolk sac tumour with antibodies against nuclear protein in testis (NUT) and two cancer/testis antigens, GAGE7 and NY-ESO-1. When tumour positivity was defined as an extent plus intensity score of ≥ 4, NUT was positive in 71% of SSs, 19% of seminomas, and 5% of solid yolk sac tumours. GAGE7 was positive in 67% of SSs and 4% of seminomas. NY-ESO-1 was positive in 82% of SSs, 13% of seminomas, and 5% of solid yolk sac tumours. The sensitivity and specificity, respectively, of these antibodies for SSs were as follows: NUT, 71% and 92%; GAGE7, 67% and 99%; and NY-ESO-1, 82% and 94%. When positivity criteria were stricter, NUT and GAGE7 positivity occurred exclusively in SS, but the sensitivity decreased to 41% and 60%, respectively, and NY-ESO-1 was 59% sensitive and 97% specific. Neither the sarcomatous component of three SSs nor any embryonal carcinoma showed reactivity with any antibody. All three antibodies are variably sensitive for SS, and high specificity is attained when there is multifocal and strong nuclear labelling.

Expression of Protein Gene Product 9.5 and Sal-like Protein 4 in Canine Seminomas

The aim of the present study was to characterize canine classical seminoma (SE) and spermatocytic seminoma (SS) by immunohistochemical expression of gonocytic and spermatogonial cellular markers (c-Kit, placental alkaline phosphatase [PLAP], protein gene product 9.5 [PGP9.5]and Sal-like protein 4 [Sall4]) and histochemically by the periodic acid-Schiff (PAS) reaction. Twenty-five cases of SE and 23 cases of SS were investigated. Two cases of dysgerminoma were also examined. c-Kit was expressed on the cell membrane of 13 of 25 cases of SE (52%) and four of 23 cases of SS (16%). This marker was not expressed in dysgerminoma. PLAP immunoreactivity was observed in the cytoplasm of neoplastic cells of six of 25 cases of SE (24%). PLAP was not expressed in cases of SS and dysgerminoma. All samples of SE, SS and dysgerminoma showed cytoplasmic expression of PGP9.5 and nuclear immunoreactivity for Sall4. There was fine granular cytoplasmic PAS staining in neoplastic cells in five of 25 cases of SE (20%), while all samples of SS and dysgerminoma cases were PAS negative. These findings suggest that it is not possible to differentiate canine SE and SS using these markers. This may be because canine SS may be derived from spermatogonia that can differentiate to spermatocytesand also because cases of canine SE might consist of neoplastic cells that have lost their gonocytic nature. This study was the first to show positive immunoreactivity for Sall4 in canine seminomas and dysgerminomas and expression of PGP9.5 in canine dysgerminomas.

Expression of human chorionic gonadotropin in testicular germ cell tumors

BackgroundWe have shown that most patients with seminomas have elevated serum concentrations of the free β subunit of human chorionic gonadotropin (hCGβ) and that in nonseminomatous testicular cancer, most of the hCG in the serum is hyperglycosylated (hCG-h). However, the tissue expression of hCG-h or hCGβ in germ cell tumors (GCTs) has not been reported. Our objective was to study the expression and diagnostic value of hCG-h and hCGβ in testicular GCTs. MethodsWe studied the immunohistochemical expression of hCG, hCG-h, hCGβ, and the free α subunit of hCG (hCGα) in GCTs from 154 patients. We compared the tissue expression with serum concentrations and evaluated the correlation between staining intensity, established prognostic variables, and outcome. ResultsThe expression varied between tumor types. All forms of hCG, including hCG-h, were detected in embryonal carcinomas (22%) and mixed GCTs (48%). Polyclonal hCG and monoclonal hCGβ antibodies detected immunoreactivity in some seminomas (7%). No form of hCG was found in spermatocytic seminomas, pure teratomas, or a yolk sac tumor. The serum concentrations correlated with the corresponding tumor expression. The staining intensities of hCG, hCGβ, hCG-h, and hCGα correlated with disease stage but not significantly with relapse, disease-related mortality, or progression-free survival. ConclusionTrophoblastic tissue expresses hCG, hCG-h, and free subunits together whereas seminoma tissue occasionally expresses hCGβ. This difference might aid in differential diagnosis of some difficult-to-classify cases.

Testicular cancer: biology and biomarkers

The term "human germ cell tumors" (GCTs) refers to a heterogeneous group of neoplasms, all with a defined histological appearance. They have specific epidemiological characteristics, clinical behavior, and pathogenesis. Histologically, GCTs contain various tissue elements, which are homologs of normal embryogenesis. We have proposed a subclassification of GCTs in five subtypes, three of which preferentially occur in the testis. These include teratomas and yolk sac tumors of neonates and infants (type I), seminomas and nonseminomas of (predominantly) adolescents and adults (type II), and spermatocytic seminomas of the elderly (type III). Both spontaneous and induced animal models have been reported, of which the relevance for human GCTs is still to be clarified. Multidisciplinary studies have recently shed new light on the (earliest steps in the) pathogenesis of GCTs, mainly in regard of malignant type II GCTs (germ cell cancer (GCC)). This review discusses novel understanding of the pathogenesis of (mainly) GCC, focusing on identification of informative diagnostic markers suitable for application in a clinical setting. These include OCT3/4, SOX9/FOXL2, SOX17/SOX2, as well as embryonic microRNAs. These markers have been identified through studies on normal embryogenesis, specifically related to the gonads, including the germ cell lineage. Their strengths and limitations are discussed as well as the expected future approach to identify the group of individuals at highest risk for development of a GCC. The latter would allow screening of defined populations, early diagnosis, optimal follow-up, and potentially early treatment, preventing long-term side effects of systemic treatment.

An autopsy study of synchronous intratesticular and mediastinal sarcoma with pulmonary metastasis

Most testicular sarcomas arise from germ cell tumors (GCTs) viz. teratoma or spermatocytic seminoma. Pure intratesticular sarcomas are very rare. We present an autopsy report of non-germ cell primary intratesticular sarcoma with synchronous mediastinal sarcoma and lung metastasis in a young male who presented with symptoms of mediastinal compression and simultaneously had a significant gradually enlarging testicular mass.

Diagnosing seminoma: practicalities and problems

Classical seminoma is the most commonly encountered testicular neoplasm. Most clinically localised seminomas are now managed by surveillance, though adjuvant chemo or radiotherapy can be given. The diagnosis of seminoma can be relatively straightforward, but may present unforseen challenges leading to inappropriate treatment or serious misdiagnosis in a number of ways. 1) Thorough macroscopy. Seminomas require rigorous blocking. This is because tiny amounts of non-seminoma may be missed, leading to potential under-treatment. Inflammatory lesions and granulomatous lesions may also harbour small foci of seminoma and should be treated with suspicion. 2) Unusual histological patterns. Some seminomas show unusual features. They may show frequent syncytiotrophoblastic cells leading to misdiagnosis as choriocarcinoma. A minority show tubular elements or even signet ring change. 3) Mimicks. Solid type yolk sac tumour may mimic seminoma as well as a number of other entities, especially some malignant sex cord stromal tumours. The former should be considered for adjuvant treatment, while the latter may require a prophylactic retroperitoneal lymph node dissection. Spermatocytic seminoma, especially when monomorphic may be mistaken for seminoma. Close morphological inspection allied to to judicious use of immunochemistry and knowledge of clinical details including serology is essential for the accurate diagnosis of seminoma.